Collagen-induced arthritis (CIA) is an experimental model of rheumatoid arthritis (RA) and has aided research into the pathogenesis of inflammatory joint disease. Typically, Type II collagen (CII) emulsified with Freund's complete adjuvant (FCA) is injected into DBA/1 mice. After a booster injection, the mice develop inflammation of the paws. But the fact that the immunization of CII alone does not induce arthritis suggests that activation of the immune system by an adjuvant is necessary for induction of the arthritis. In the present study, we investigated the ability of beta-glucans derived from Candida albicans to act as an adjuvant to induce autoimmune arthritis. DBA/1 mice were injected with CII emulsified with FCA or particulate beta-glucan, OX-CA, on day 0 and given a booster at day 21. Mice immunized with CII plus OX-CA developed arthritis at around 7-10 days after the booster injection. Similarly, mice administered CII emulsified with FCA developed arthritis with the same time course. The mice immunized with CII and OX-CA had a more severe arthritis than those immunized with CII and FCA. Histological changes and production of anti-CII antibody were observed regardless of the type of injection. In addition, components of C. albicans were also tested for their ability to induce arthritis as an adjuvant. The results showed that CSBG, which is a soluble beta-glucan, acted as an adjuvant for CIA but CAWS, which is a mannoprotein-beta-glucan complex, did not. In conclusion, beta-glucan derived from C. albicans acted as an adjuvant and the injection with CII resulted in arthritis with the production of anti-CII autoantibody. The results strongly suggested that fungal metabolites such as beta-glucans have the capacity to induce and exacerbate autoimmune diseases such as RA.